Case Presentation: A 31-year-old-female presented to the hospital with a one-day history of severe left lower quadrant abdominal pain that was gradual in onset, associated with nausea and emesis. She also reported epigastric and left flank pain. She experienced a similar episode two months prior, which lasted several days. She denied hematuria, vaginal discharge, or history of urinary tract infections. Review of systems was otherwise negative. She denied personal or family history of lipid disorders or pancreatitis. She denied any alcohol use. Her vitals were normal. Exam was notable for severe left lower quadrant and left flank tenderness to palpation with voluntary guarding, and moderate tenderness in the epigastrium and left upper quadrant. Labs were remarkable for a white blood cell count of 12.1 k/μL without left shift. A comprehensive metabolic panel, urinalysis, lipase, urine gonorrhea and chlamydia assays, and vaginal wet and KOH prep were normal. CT of the abdomen and pelvis was notable for fluid stranding surrounding the tail of the pancreas. MRCP revealed gallstones and peripancreatic edema but no evidence of obstruction, mass, or cysts. A transvaginal ultrasound was unremarkable. The patient was admitted for suspected acute pancreatitis and treated with bowel rest and intravenous fluids. The following day, a lipid panel was obtained, revealing off-scale, severe hypertriglyceridemia, subsequently quantified at 7644 mg/dL. She was treated with fixed dose intravenous insulin infusion at 0.1 units/kg/hr along with dextrose infusion, which was maintained for three days until triglycerides were below 600 mg/dL. Her symptoms gradually improved, and she was discharged on fenofibrate.
Discussion: This case is remarkable for treatment of a relatively uncommon cause of pancreatitis, as well as atypical presentation of symptoms. Hypertriglyceridemia-induced pancreatitis (HTGP) occurs in 1-14% of cases of acute pancreatitis, with alcohol-induced or gallstone pancreatitis being the most common etiologies. Hypertriglyceridemia can be primary, caused by genetic disorders, or secondary, caused by autoimmune disorders, medications, alcohol, or pregnancy. The typical presentation for acute pancreatitis includes acute or gradual onset epigastric pain that can radiate to the back. Laboratory markers of acute pancreatitis include an elevated serum amylase and/or serum lipase. Treatment for HTGP includes initiation of an insulin drip at 0.1-0.3 units/kg/hr, versus plasmapheresis if there are signs of worrisome features, such as organ dysfunction. Treatment with insulin requires careful attention for signs of hypoglycemia and for signs of fluid overload, as patients may receive large amounts of dextrose to combat hypoglycemia. Caution should be given to patients that are insulin naive, and in this case, we proceeded with more conservative treatment. Finally, triglycerides greater than 500 mg/dl pose a higher risk for recurrence of HTGP, and prevention requires multimodal therapy, including lifestyle changes and medication. Fibrates are more effective in lowering triglyceride levels compared with statins, however, caution must be taken with fibrates as they can predispose to gallstone formation and increase the risk of pancreatitis.
Conclusions: There is no definitive standard for management of HTGP, and many hospitals lack protocols for treatment. Long term treatment itself can pose a risk of recurrent episodes of HGTP. Further studies are needed in order to provide precise treatment recommendations.